ArticlePloS one2016
Hippocampal Fast Glutamatergic Transmission Is Transiently Regulated by Corticosterone Pulsatility.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 33 citations in OpenAlex.
- The Size and Localization of Ribeye and GluR2 in the Auditory Inner Hair Cell Synapse of C57BL/6 Mice Are Affected by Short-Pulse Corticosterone in a Sex-Dependent Manner.Brain sciences · 2025Article
- Mitogen-activated protein kinase dependent presynaptic potentiation in the lateral habenula mediates depressive-like behaviors in rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- A Scoping Review of Corticosterone-Induced Changes in Ionotropic Glutamate Receptor Levels and Localization in the Rodent Brain: Implications for the Auditory System.Brain sciences · 2025Review
- Acute deletion of the central MR/GR steroid receptor correlates with changes in LTP, auditory neural gain, and GC-A cGMP signaling.Frontiers in molecular neuroscience · 2023Article
- Multiplexed Membrane Signaling by Glucocorticoids.Current opinion in endocrine and metabolic research · 2022Article
- Brain mineralocorticoid receptor in health and disease: From molecular signalling to cognitive and emotional function.British journal of pharmacology · 2022Article
- Top-down and bottom-up control of stress-coping.Journal of neuroendocrinology · 2019Review
- Relationship between Cytotoxicity in the Hippocampus and an Abnormal High Intensity Area on the Diffusion-weighted Images of Three Patients with Transient Global Amnesia.Internal medicine (Tokyo, Japan) · 2018Article
- Effect of Ketamine on LTP and NMDAR EPSC in Hippocampus of the Chronic Social Defeat Stress Mice Model of Depression.Frontiers in behavioral neuroscience · 2018Article
- Stress hormone rapidly tunes synaptic NMDA receptor through membrane dynamics and mineralocorticoid signalling.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years it has become clear that corticosteroid hormones (such as corticosterone) are released in ultradian pulses as a natural consequence of pituitary-adrenal interactions. All organs, including the brain, are thus exposed to pulsatile changes in corticosteroid hormone level, important to ensure full genomic responsiveness to stress-induced surges. However, corticosterone also changes neuronal excitability through rapid non-genomic pathways, particularly in the hippocampus. Potentially, background excitability of hippocampal neurons could thus be changed by pulsatile exposure to corticosteroids. It is currently unknown, though, how neuronal activity alters during a sequence of corticosterone pulses. To test this, hippocampal cells were exposed in vitro to four consecutive corticosterone pulses with a 60 min inter-pulse interval. During the pulses we examined four features of hippocampal signal transfer by the main excitatory transmitter glutamate-i.e., postsynaptic responses to spontaneous release of presynaptic vesicles, postsynaptic GluA2-AMPA receptor dynamics, basal (evoked) field responses, and synaptic plasticity, using a set of high resolution imaging and electrophysiological approaches. We show that the first pulse of corticosterone causes a transient increase in miniature EPSC frequency, AMPA receptor trafficking and synaptic plasticity, while basal evoked field responses are unaffected. This pattern is not maintained during subsequent applications: responses become more variable, attenuate or even reverse over time, albeit with different kinetics for the various experimental endpoints. This may indicate that the beneficial effect of ultradian pulses on transcriptional regulation in the hippocampus is not consistently accompanied by short-term perturbations in background excitability. In general, this could be interpreted as a means to keep hippocampal neurons responsive to incoming signals related to environmental challenges.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.